Our assay method does not require HBV infection or radioactive <sup>3</sup>H-TCA and provides a facile way to identify viral entry inhibitors via measuring bile acid transport activity of NTCP.
Human NTCP transgenic mouse still could not support productive HBV infection, and humanized mouse liver with human hepatocytes which supported whole HBV life cycle still dominates HBV infection in vivo, a value but expensive model until now.
CXCR5<sup>+</sup>CD8<sup>+</sup>T cells are partially exhausted while possess a more potent antiviral activity through producing high levels of HBV-specific IFN-γ and IL-21 in chronic HBV infection.
Sodium taurocholate cotransporting polypeptide (NTCP) is expressed at the surface of human hepatocytes and functions as an entry receptor of hepatitis B virus (HBV).
The in vitro HBV infection assay system was established in primary human hepatocytes infected with HBV derived from the plasmid containing 1.3-mer HBV genome, and treated with IFN-γ.
Evolution of Hepatitis B Virus Receptor NTCP Reveals Differential Pathogenicities and Species Specificities of Hepadnaviruses in Primates, Rodents, and Bats.
This study demonstrated, for the first time, that ADAR1 plays an antiviral role against HBV infection by increasing the level of miRNA-122 in hepatocytes.
When correlating miRNA expression with clinical parameters we detected significant association between hepatitis B virus (HBV) infection and miR-122 in serum as well as several serum and tissue-miRNAs that correlated with surgery type.
The IFN-β-Luc expression and level of hepatitis B virus surface Antigen (HBsAg) showed that DDX3 mediated by the 5-HT<sub>7</sub> agonist (AS-19) increased IFN-β expression and inhibited HBV replication.
However, the researches on the accuracy of miR122 detection in chronic viral hepatitis have been inconsistent, leading us to conduct this meta-analysis to systematically summarize the diagnostic value of circulating miR-122 in patients with hepatitis B virus (HBV) and/or hepatitis C virus (HCV)-associated chronic viral hepatitis.<b>Methods:</b> A comprehensive literature search (updated to January 30, 2019) in PubMed, Cochrane library, EMBASE, CNKI, Wanfang, and CQVIP databases was performed to identify eligible studies.
Moreover, the aa 158 sequence determined attachment of the HBV envelope protein to the host cell, demonstrating the mechanism whereby HBV infection would create positive selection at this NTCP residue.
Inhibition of miR-3613-3p decreased relative expressions of IFN-α and IFN-β, HBV DNA copies, and increased the hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) levels, whereas miR-3613-3p overexpression reversed these changes in vitro and in vivo.
Collectively, the findings of the present study may provide insight into the mechanistic role of HBV infection in modulating the expression of miR‑122, which targets the 3'UTR of APOBEC2 mRNA, subsequently inducing liver carcinogenesis.
Identification of sodium taurocholate cotransporting polypeptide (NTCP) as an entry receptor for hepatitis B and D viruses (HBV and HDV) has not only promoted our understanding of the mechanism underlying the viral entry process, but also provided cell culture models supporting viral infection.
Here, we modified synthetic lipid-based nanoparticles with targeting peptides derived from the hepatitis B virus large envelope protein (HBVpreS) to specifically target the sodium-taurocholate cotransporting polypeptide (NTCP; <i>SLC10A1</i>) on the sinusoidal membrane of hepatocytes.
Conclusion: These findings highlight a host gene, UBE2L3, contributing to the susceptibility to persistent HBV infection; UBE2L3 may be involved in IFN-mediated viral suppression and serve as a potential target in the prevention and treatment of HBV infection.
In addition, the expression of IFN-γ and PD-L1 in the colon was found to be up-regulated early in mice with acute HBV infection, whereas the expression of PD-L1 in the colon of mice with chronic HBV infection was up-regulated later.
In summary, our study suggests that HBV precore protein, specifically the p22 form, impedes JAK-STAT signaling to help the virus evade the host innate immune response and, thus, causes resistance to IFN therapy.<b>IMPORTANCE</b> Chronic hepatitis B virus (HBV) infection continues to be a major global health concern, and patients who fail to mount an efficient immune response to clear the virus will develop a life-long chronic infection that can progress to chronic active hepatitis, cirrhosis, and primary hepatocellular carcinoma.
Identifying the key negative factors and elucidating the regulating mechanism are essential for improving anti-HBV (hepatitis B virus) efficacy of IFNα.